NDRG2 inhibition facilitates angiogenesis of hepatocellular carcinoma

Hepatocellular carcinoma (HCC) is an angiogenesis-dependent tumor, and angiogenesis plays pivotal roles in progression and hematogenous metastasis. Upregulating NDRG2 expression could inhibit endothelial cell proliferation and tumor angiogenesis. However, the development of angiogenesis is a complic...

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Autores principales:	Wang Jianlong, Li Tao, Ma Lifeng, Liu Guochao, Wang Guiying, Kang Jiansheng
Formato:	article
Lenguaje:	EN
Publicado:	De Gruyter 2021
Materias:	hepatocellular carcinoma ndrg2 angiogenesis vegfa Medicine R
Acceso en línea:	https://doaj.org/article/a21ced18cd00455aa1f70999f337211f
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spelling	oai:doaj.org-article:a21ced18cd00455aa1f70999f337211f2021-12-05T14:10:54ZNDRG2 inhibition facilitates angiogenesis of hepatocellular carcinoma2391-546310.1515/med-2021-0268https://doaj.org/article/a21ced18cd00455aa1f70999f337211f2021-05-01T00:00:00Zhttps://doi.org/10.1515/med-2021-0268https://doaj.org/toc/2391-5463Hepatocellular carcinoma (HCC) is an angiogenesis-dependent tumor, and angiogenesis plays pivotal roles in progression and hematogenous metastasis. Upregulating NDRG2 expression could inhibit endothelial cell proliferation and tumor angiogenesis. However, the development of angiogenesis is a complicated and dynamic process, and the specific mechanisms that NDRG2 influences its progression are largely unknown. Conditioned media (CM) was collected from HCC cells. Cell viability, migration assay, tube formation, and western blot were used to evaluate the effect of NDRG2 on angiogenesis in HCC cells. ELISA assay was used to measure the level of VEGFA in CM. CM from NDRG2 knockdown cells significantly promoted HUVECs proliferation, migration, and tube formation compared with control cells. The level of VEGFA in CM was increased by NDRG2 knockdown relative to the control group. The expression of VEGFA, HIF-1α, and p-Akt was significantly increased in NDRG2 knockdown cells. CM from NDRG2 knockdown cells with VEGFA antibody failed to induce HUVEC proliferation, migration, and tube formation. YC-1 significantly inhibited the level of VEGFA in CM from NDRG2 knockdown cells. YC-1 also inhibited the expression of VEGFA and HIF-1α. Therefore, NDRG2 inhibition promoted the angiogenesis of HCC via VEGFA and may be used to be an anti-angiogenesis target.Wang JianlongLi TaoMa LifengLiu GuochaoWang GuiyingKang JianshengDe Gruyterarticlehepatocellular carcinomandrg2angiogenesisvegfaMedicineRENOpen Medicine, Vol 16, Iss 1, Pp 742-748 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	hepatocellular carcinoma ndrg2 angiogenesis vegfa Medicine R
spellingShingle	hepatocellular carcinoma ndrg2 angiogenesis vegfa Medicine R Wang Jianlong Li Tao Ma Lifeng Liu Guochao Wang Guiying Kang Jiansheng NDRG2 inhibition facilitates angiogenesis of hepatocellular carcinoma
description	Hepatocellular carcinoma (HCC) is an angiogenesis-dependent tumor, and angiogenesis plays pivotal roles in progression and hematogenous metastasis. Upregulating NDRG2 expression could inhibit endothelial cell proliferation and tumor angiogenesis. However, the development of angiogenesis is a complicated and dynamic process, and the specific mechanisms that NDRG2 influences its progression are largely unknown. Conditioned media (CM) was collected from HCC cells. Cell viability, migration assay, tube formation, and western blot were used to evaluate the effect of NDRG2 on angiogenesis in HCC cells. ELISA assay was used to measure the level of VEGFA in CM. CM from NDRG2 knockdown cells significantly promoted HUVECs proliferation, migration, and tube formation compared with control cells. The level of VEGFA in CM was increased by NDRG2 knockdown relative to the control group. The expression of VEGFA, HIF-1α, and p-Akt was significantly increased in NDRG2 knockdown cells. CM from NDRG2 knockdown cells with VEGFA antibody failed to induce HUVEC proliferation, migration, and tube formation. YC-1 significantly inhibited the level of VEGFA in CM from NDRG2 knockdown cells. YC-1 also inhibited the expression of VEGFA and HIF-1α. Therefore, NDRG2 inhibition promoted the angiogenesis of HCC via VEGFA and may be used to be an anti-angiogenesis target.
format	article
author	Wang Jianlong Li Tao Ma Lifeng Liu Guochao Wang Guiying Kang Jiansheng
author_facet	Wang Jianlong Li Tao Ma Lifeng Liu Guochao Wang Guiying Kang Jiansheng
author_sort	Wang Jianlong
title	NDRG2 inhibition facilitates angiogenesis of hepatocellular carcinoma
title_short	NDRG2 inhibition facilitates angiogenesis of hepatocellular carcinoma
title_full	NDRG2 inhibition facilitates angiogenesis of hepatocellular carcinoma
title_fullStr	NDRG2 inhibition facilitates angiogenesis of hepatocellular carcinoma
title_full_unstemmed	NDRG2 inhibition facilitates angiogenesis of hepatocellular carcinoma
title_sort	ndrg2 inhibition facilitates angiogenesis of hepatocellular carcinoma
publisher	De Gruyter
publishDate	2021
url	https://doaj.org/article/a21ced18cd00455aa1f70999f337211f
work_keys_str_mv	AT wangjianlong ndrg2inhibitionfacilitatesangiogenesisofhepatocellularcarcinoma AT litao ndrg2inhibitionfacilitatesangiogenesisofhepatocellularcarcinoma AT malifeng ndrg2inhibitionfacilitatesangiogenesisofhepatocellularcarcinoma AT liuguochao ndrg2inhibitionfacilitatesangiogenesisofhepatocellularcarcinoma AT wangguiying ndrg2inhibitionfacilitatesangiogenesisofhepatocellularcarcinoma AT kangjiansheng ndrg2inhibitionfacilitatesangiogenesisofhepatocellularcarcinoma
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NDRG2 inhibition facilitates angiogenesis of hepatocellular carcinoma

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